This study offers a simple and robust cellular bioassay to predict survival in metastatic melanoma patients receiving immunotherapy at early times in their treatment by integrating multiple functions that mediate effective immune response.

Use of a novel in vivo multimodal imaging system reveals that seeding of lymphoma cells into peripheral lymph nodes occurs by a rapid release of large numbers of tumor cells from the spleen or bone marrow, in contrast to the accepted paradigm of metastatic seeding.

Renal cancer is thought to be a highly immunogenic cancer, but it has been difficult to identify and understand the nature of the tumor-infiltrating lymphocytes before this study, which has implications for understanding the role of T-cell memory in effective immune responses in cancer.

Within breast tumors, interaction between the ICOS receptor on infiltrating T cells with the ICOS ligand on infiltrating plasmacytoid dendritic cells is a pivotal determinant of immune escape and is strongly rationalized as a therapeutic target to combine with other treatments.

Most incident HPV infection appears to be attributable to past sexual behavior at older ages, supporting a natural history model of viral latency and reactivation, which must be considered in developing recommendations for cervical cancer screening, as more highly exposed women transition through menopause in coming decades.

Findings suggest that an approved antibiotic drug might be immediately repositioned to enhance the effectiveness of DNA-damaging chemotherapies used widely as first-line treatment of metastatic cancer.

Toll-like receptors are thought to operate as proinflammatory receptors in immune cells, but this study lends credence to the idea that their frequent overexpression on cancer cells also has functional import, with potential prognostic and therapeutic implications.

This study provides mechanistic insights into an important pathway of metastasis in melanoma, one of the most aggressive cancers, possibly stimulating new therapeutic strategies to block or reverse this process in patients.

This study provides proof-of-concept for use of a modified lentiviral-mediated gene therapy to destroy lung tumors, where expression of the therapeutic gene is controlled by a powerful antioxidant response element that is strongly upregulated in the cancer cells.

The study revealed that a low level expression of the tumor suppressor p21 is maintained by an evolutionary-conserved repression element that can be turned “on” by selected chemotherapeutic drugs to slow cancer growth.

A natural product that activates the integrated stress response and modulates TH17 immunity is shown here to block TGF-β induced signals that drive bone and brain metastasis in melanoma, suggesting therapeutic applications of this compound for therapy of advanced forms of this disease.

An important B cell regulatory factor identified as a key Ras effector is found to connect Ras and TGF-β signaling pathways, which coordinate EMT in cancer cells, a hallmark of invasion and metastatic behaviors.

This important study suggests that precancerous lesions have already evolved a mutator phenotype that can drive malignant progression and also reveals mechanistic insights into how point mutations accumulate.